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WormBase Tree Display for Gene: WBGene00005008

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Name Class

WBGene00005008EvidencePaper_evidenceWBPaper00005903
SMapS_parentSequenceC07A12
IdentityVersion1
NameCGC_namespr-3Person_evidenceWBPerson220
Sequence_nameC07A12.5
Molecular_nameC07A12.5a
C07A12.5a.1
CE36266
C07A12.5b
CE53297
C07A12.5b.1
Other_nameCELE_C07A12.5Accession_evidenceNDBBX284606
Public_namespr-3
DB_infoDatabaseAceViewgeneXF135
WormQTLgeneWBGene00005008
WormFluxgeneWBGene00005008
OMIMgene600571
NDBlocus_tagCELE_C07A12.5
PanthergeneCAEEL|WormBase=WBGene00005008|UniProtKB=Q17768
familyPTHR24403
NCBIgene180722
RefSeqproteinNM_001373281.4
NM_001029196.5
SwissProtUniProtAccQ17768
UniProt_GCRPUniProtAccQ17768
SpeciesCaenorhabditis elegans
HistoryVersion_change107 Apr 2004 11:29:37WBPerson1971EventImportedInitial conversion from geneace
StatusLive
Gene_info (10)
Disease_infoExperimental_modelDOID:10652Homo sapiensPaper_evidenceWBPaper00045043
Curator_confirmedWBPerson324
Date_last_updated21 Oct 2014 00:00:00
Disease_relevanceHuman RE1-silencing transcription factor (REST), also known as Neuron-restrictive silencer factor (NRSF) is a transcriptional repressor, also involved in repression of neuronal genes during embryonic development that is down-regulated after terminal neuronal differentiation; recent transcriptional profiling data indicate that REST is induced in the aging brain and declines in Alzhemier''s disease (AD); REST is neuroprotective, repressing genes involved in cell death and strongly inhibiting tau phosphorylation, associated with AD; REST-deficient mice showed a progressive age-related neurodegenerative phenotype; in C. elegans, mutations in the multi-zinc finger transcripton factors, spr-3 and spr-4, structurally resembling mammalian REST, and a mutation in spr-1, orthologous to CoREST, showed significantly reduced survival relative to wild-type controls, with spr-4(by105) most affected; further, transgenic expression of human REST could functionally replace wild-type spr-4, as indicated by reducing paraquat-induced elevated ROS levels in spr-4(by105) and by repressing the presenilin gene hop-1, which is repressed by SPR-4; SPR-4 also modulated the neurotoxicity of A-beta in an C. elegans line that expresses A-beta42 in glutamatergic neurons and undergoes age-dependent neuronal loss, when this line was crossed with the spr-4(by105) mutant, the resulting line expressed A-beta42 and showed significantly accelerated neurodegeneration; thus, SPR-4 protects against both oxidative stress and A-beta toxicity, consistent with a general role in stress resistance.Homo sapiensPaper_evidenceWBPaper00045043
Accession_evidenceOMIM600571
Curator_confirmedWBPerson324
Date_last_updated22 Oct 2014 00:00:00
Models_disease_assertedWBDOannot00000800
Molecular_infoCorresponding_CDSC07A12.5a
C07A12.5b
Corresponding_CDS_historyC07A12.5:wp81
C07A12.5:wp114
C07A12.5b:wp271
Corresponding_transcriptC07A12.5a.1
C07A12.5b.1
Associated_featureWBsf648017
WBsf648018
WBsf1004973
WBsf1004974
WBsf1022801
WBsf1022802
WBsf235588
Transcription_factorWBTranscriptionFactor000627
Experimental_infoRNAi_resultWBRNAi00113378Inferred_automaticallyRNAi_primary
WBRNAi00114341Inferred_automaticallyRNAi_primary
WBRNAi00067551Inferred_automaticallyRNAi_primary
WBRNAi00000791Inferred_automaticallyRNAi_primary
WBRNAi00039964Inferred_automaticallyRNAi_primary
WBRNAi00010358Inferred_automaticallyRNAi_primary
Expr_patternExpr2603
Expr2604
Expr2605
Expr9762
Expr9770
Expr1027050
Expr1032492
Expr1144043
Expr2016090
Expr2034325
Drives_constructWBCnstr00010865
WBCnstr00014282
WBCnstr00014290
WBCnstr00035271
Construct_productWBCnstr00035271
WBCnstr00038836
Microarray_results (23)
Expression_cluster (142)
Interaction (18)
Map_infoMapXPosition-7.38771Error0.016176
PositivePositive_cloneC07A12Inferred_automaticallyFrom sequence, transcript, pseudogene data
Mapping_dataMulti_point4256
4692
Pseudo_map_position
Reference (19)
Remarkpublished in Wen et al., PNAS 97: 14527-14529, 2000
Map position created from combination of previous interpolated map position (based on known location of sequence) and allele information. Therefore this is not a genetic map position based on recombination frequencies or genetic experiments. This was done on advice of the CGC.CGC_data_submission
MethodGene